Context: There has been renewed interest in anti-Mü llerian hormone (AMH) because of its role in the ovary. Data on its actions are sparse, but it appears to inhibit follicle growth. Interestingly, serum AMH is two to three times higher in women with polycystic ovary (PCO) syndrome than women with normal ovaries. Objective:We examined the production of AMH by cells from a range of follicle sizes from normal ovaries and compared this with production by ovulatory and anovulatory (anov) PCOs.Design: Granulosa cells (GCs) and theca and follicular fluid (ff) were isolated from intact follicles. Cells were cultured for 48 h Ϯ FSH or LH, and AMH was measured in ff and cell-conditioned media (CM).Results: AMH levels in ff and GC-CM ranged from 42 to 2240 and 0.025 to 1.7 ng/ml, respectively, and were low or undetectable in ff and GC-CM from follicles greater than 9 mm, luteinized cells, and theca and stroma. The mean level of AMH was four times higher in GC-CM from ovulatory PCOs [mean (range) 1.56 (0.025-7)] and 75 times higher from anovPCO [21.4 (17.2-43 ng/ml)] than normal ovaries [0.37 (0.025-1.7)]. Neither LH nor FSH had an effect on AMH production by GCs from normal ovaries, but in cells from PCOs, FSH significantly decreased AMH, and in contrast, LH increased AMH. Conclusions:The reduction of AMH in follicles greater than 9 mm from normal ovaries appears to be an important requirement for the selection of the dominant follicle. AMH production per GC was 75 times higher in anovPCOs, compared with normal ovaries. This increase in AMH may contribute to failure of follicle growth and ovulation seen in polycystic ovary syndrome.

The low prevalence of MALA is comparable to the prevalence of sulphonylurea-induced hypoglycaemia. Metformin has many beneficial metabolic effects in the management of Type 2 diabetes mellitus. Provided that the recommended guidelines for metformin use are strictly adhered to, its widespread use would be safe and the incidence of MALA will be further reduced.

A 29-year-old patient presented with bilateral pulmonary lesions following surgery for recurrent placental site trophoblastic tumor (PSTT). On day seven after institution of the 'EMA' regimen (etoposide, medium dose methotrexate with folinic acid rescue and actinomycin-D), complete pneumothorax occurred. Closed-system air drainage brought only transient lung expansion and subsequent talc pleurodesis was needed. During follow-up, complete regression of lung metastases was observed. A literature survey of post-chemotherapy pneumothorax in patients with lung metastases disclosed fourteen hitherto reported cases. Including the present PSTT case, non-epithelial gynecologic malignancy (3 patients) ranks second to osteogenic sarcoma (6 cases) with regard to the primary tumor involved.

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